110 research outputs found
Impaired coronary blood flow at higher heart rates during atrial fibrillation: investigation via multiscale modelling
Background. Different mechanisms have been proposed to relate atrial
fibrillation (AF) and coronary flow impairment, even in absence of relevant
coronary artery disease (CAD). However, the underlying hemodynamics remains
unclear. Aim of the present work is to computationally explore whether and to
what extent ventricular rate during AF affects the coronary perfusion.
Methods. AF is simulated at different ventricular rates (50, 70, 90, 110, 130
bpm) through a 0D-1D multiscale validated model, which combines the left
heart-arterial tree together with the coronary circulation. Artificially-built
RR stochastic extraction mimics the \emph{in vivo} beating features. All the
hemodynamic parameters computed are based on the left anterior descending (LAD)
artery and account for the waveform, amplitude and perfusion of the coronary
blood flow.
Results. Alterations of the coronary hemodynamics are found to be associated
either to the heart rate increase, which strongly modifies waveform and
amplitude of the LAD flow rate, and to the beat-to-beat variability. The latter
is overall amplified in the coronary circulation as HR grows, even though the
input RR variability is kept constant at all HRs.
Conclusions. Higher ventricular rate during AF exerts an overall coronary
blood flow impairment and imbalance of the myocardial oxygen supply-demand
ratio. The combined increase of heart rate and higher AF-induced hemodynamic
variability lead to a coronary perfusion impairment exceeding 90-110 bpm in AF.
Moreover, it is found that coronary perfusion pressure (CPP) is no longer a
good measure of the myocardial perfusion for HR higher than 90 bpm.Comment: 8 pages, 5 figures, 3 table
Alteration of cerebrovascular haemodynamic patterns due to atrial fibrillation: an in silico investigation
There has recently been growing evidence that atrial fibrillation (AF), the
most common cardiac arrhythmia, is independently associated with the risk of
dementia. This represents a very recent frontier with high social impact for
the number of individuals involved and for the expected increase in AF
incidence in the next 40 years. Although a number of potential haemodynamic
processes, such as microembolisms, altered cerebral blood flow, hypoperfusion
and microbleeds, arise as connecting links between the two pathologies, the
causal mechanisms are far from clear. An in silico approach is proposed that
combines in sequence two lumped-parameter schemes, for the cardiovascular
system and the cerebral circulation. The systemic arterial pressure is obtained
from the cardiovascular system and used as the input for the cerebral
circulation, with the aim of studying the role of AF on the cerebral
haemodynamics with respect to normal sinus rhythm (NSR), over a 5000 beat
recording. In particular, the alteration of the haemodynamic (pressure and
flowrate) patterns in the microcirculation during AF is analysed by means of
different statistical tools, from correlation coefficients to autocorrelation
functions, crossing times, extreme values analysis and multivariate linear
regression models. A remarkable signal alteration, such as a reduction in
signal correlation (NSR, about 3 s; AF, less than 1 s) and increased
probability (up to three to four times higher in AF than in NSR) of extreme
value events, emerges for the peripheral brain circulation. The described
scenario offers a number of plausible cause-effect mechanisms that might
explain the occurrence of critical events and the haemodynamic links relating
to AF and dementia.Comment: 13 pages, 9 Figures, 3 Table
Rate Control Management of Atrial Fibrillation: May a Mathematical Model Suggest an Ideal Heart Rate?
Background. Despite the routine prescription of rate control therapy for
atrial fibrillation (AF), clinical evidence demonstrating a heart rate target
is lacking. Aim of the present study was to run a mathematical model simulating
AF episodes with a different heart rate (HR) to predict hemodynamic parameters
for each situation.
Methods. The lumped model, representing the pumping heart together with
systemic and pulmonary circuits, was run to simulate AF with HR of 50, 70, 90,
110 and 130 bpm, respectively.
Results. Left ventricular pressure increased by 56.7%, from 33.92+-37.56 mmHg
to 53.15+-47.56 mmHg, and mean systemic arterial pressure increased by 27.4%,
from 82.66+-14.04 mmHg to 105.29+-7.63 mmHg, at the 50 and 130 bpm simulations,
respectively. Stroke volume (from 77.45+-8.5 to 39.09+-8.08 mL), ejection
fraction (from 61.1+-4.4 to 39.32+-5.42%) and stroke work (SW, from 0.88+-0.04
to 0.58+-0.09 J) decreased by 49.5, 35.6 and 34.2%, at the 50 and 130 bpm
simulations, respectively. In addition, oxygen consumption indexes (rate
pressure product, RPP, tension time index per minute, TTI/min, and pressure
volume area per minute, PVA/min) increased from the 50 to the 130 bpm
simulation, respectively, by 185.7% (from 5598+-1939 to 15995+-3219 mmHg/min),
55.5% (from 2094+-265 to 3257+-301 mmHg s/min) and 102.4% (from 57.99+-17.9 to
117.37+-25.96 J/min). In fact, left ventricular efficiency (SW/PVA) decreased
from 80.91+-2.91% at 50 bpm to 66.43+-3.72% at the 130 bpm HR simulation.
Conclusion. Awaiting compulsory direct clinical evidences, the present
mathematical model suggests that lower HRs during permanent AF relates to
improved hemodynamic parameters, cardiac efficiency, and lower oxygen
consumption.Comment: 9 page
Cardiovascular response to orthostatic stress: multiscale modeling with focus on the coronary circulation
Cardiovascular modeling has shown impressive potentialities in understanding and predicting cardio vascular system (CVS) functioning, disorders and response under several conditions. By adopting a recent closed-loop multiscale model of the entire CVS, we computationally investigated the coronary
hemodynamics response to passive orthostatic stress elicited by upright head-up tilt (HUT). Beside known CVS consequences following passive upright tilting – such as heart rate and blood pressure augmentation, stroke volume and cardiac output drop – we found that coronary blood flow (CBF) was enhanced by up to 18% at 70◦ HUT, in response to a coronary perfusion pressure (CPP) rise of 26%
Arterial wave dynamics preservation upon orthostatic stress: a modelling perspective
Pressure-flow travelling waves are a key topic for understanding
arterial haemodynamics. However, wave transmission and
reflection processes induced by body posture changes have not
been thoroughly explored yet. Current in vivo research has
shown that the amount of wave reflection detected at a central
level (ascending aorta, aortic arch) decreases during tilting to
the upright position, despite the widely proved stiffening of the
cardiovascular system. It is known that the arterial system is
optimized when in the supine position, i.e. propagation of
direct waves is enabled and reflected waves are trapped,
protecting the heart; however, it is not known whether this is
preserved with postural changes. To shed light on these
aspects, we propose a multi-scale modelling approach to
inquire into posture-induced arterial wave dynamics elicited by
simulated head-up tilting. In spite of remarkable adaptation of
the human vasculature following posture changes, our analysis
shows that, upon tilting from supine to upright: (i) vessel
lumens at arterial bifurcations remain well matched in the
forward direction, (ii) wave reflection at central level is reduced
due to the backward propagation of weakened pressure waves
produced by cerebral autoregulation, and (iii) backward wave
trapping is preserved
Higher ventricular rate during atrial fibrillation relates to increased cerebral hypoperfusions and hypertensive events
Atrial fibrillation (AF) is associated with cognitive impairment/dementia,
independently of clinical cerebrovascular events (stroke/TIA). One of the
plausible mechanisms is the occurrence of AF-induced transient critical
hemodynamic events; however, it is presently unknown, if ventricular response
rate during AF may impact on cerebral hemodynamics. AF was simulated at
different ventricular rates (50, 70, 90, 110, 130 bpm) by two coupled lumped
parameter validated models (systemic and cerebral circulation), and compared to
corresponding control normal sinus rhythm simulations (NSR). Hemodynamic
outcomes and occurrence of critical events (hypoperfusions and hypertensive
events) were assessed along the internal carotid artery-middle cerebral artery
pathway up to the capillary-venous bed. At the distal cerebral circle level
(downstream middle cerebral artery), increasing ventricular rates lead to a
reduced heart rate-related dampening of hemodynamic signals compared to NSR
(p=0.003 and 0.002 for flow rate and pressure, respectively). This response
causes a significant progressive increase in critical events in the distal
cerebral circle (p<0.001) as ventricular rate increases during AF. On the other
side, at the lowest ventricular response rates (HR 50 bpm), at the
systemic-proximal cerebral circle level (up to middle cerebral artery)
hypoperfusions (p<0.001) occur more commonly, compared to faster AF
simulations. This computational study suggests that higher ventricular rates
relate to a progressive increase in critical cerebral hemodynamic events
(hypoperfusions and hypertensive events) at the distal cerebral circle. Thus, a
rate control strategy aiming to around 60 bpm could be beneficial in terms on
cognitive outcomes in patients with permanent AF.Comment: 9 pages, 4 figures, 2 table
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